Abstract
The focal dystonia benign essential blepharospasm (BEB) affects as many as 40,000 individuals in the United States. This dystonia is characterized by trigeminal hyperexcitability, photophobia, and most disabling of the symptoms, involuntary spasms of lid closure that can produce functional blindness. Like many focal dystonias, BEB appears to develop from the interaction between a predisposing condition and an environmental trigger. The primary treatment for blepharospasm is to weaken the eyelid-closing orbicularis oculi muscle to reduce lid spasms. There are several animal models of blepharospasm that recreate the spasms of lid closure in order to investigate pharmacological treatments to prevent spasms of lid closure. One animal model attempts to mimic the predisposing condition and environmental trigger that give rise to BEB. This model indicates that abnormal interactions among trigeminal blink circuits, basal ganglia, and the cerebellum are the neural basis for BEB.
Keywords: Basal ganglia, blepharospasm, blink, cerebellum, motor adaptation, trigeminal
Current Neuropharmacology
Title:Animal Models for Investigating Benign Essential Blepharospasm
Volume: 11 Issue: 1
Author(s): Craig Evinger
Affiliation:
Keywords: Basal ganglia, blepharospasm, blink, cerebellum, motor adaptation, trigeminal
Abstract: The focal dystonia benign essential blepharospasm (BEB) affects as many as 40,000 individuals in the United States. This dystonia is characterized by trigeminal hyperexcitability, photophobia, and most disabling of the symptoms, involuntary spasms of lid closure that can produce functional blindness. Like many focal dystonias, BEB appears to develop from the interaction between a predisposing condition and an environmental trigger. The primary treatment for blepharospasm is to weaken the eyelid-closing orbicularis oculi muscle to reduce lid spasms. There are several animal models of blepharospasm that recreate the spasms of lid closure in order to investigate pharmacological treatments to prevent spasms of lid closure. One animal model attempts to mimic the predisposing condition and environmental trigger that give rise to BEB. This model indicates that abnormal interactions among trigeminal blink circuits, basal ganglia, and the cerebellum are the neural basis for BEB.
Export Options
About this article
Cite this article as:
Evinger Craig, Animal Models for Investigating Benign Essential Blepharospasm, Current Neuropharmacology 2013; 11 (1) . https://dx.doi.org/10.2174/1570159X11311010008
DOI https://dx.doi.org/10.2174/1570159X11311010008 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
- Forthcoming Thematic Issues
Related Articles
-
Blood-Brain Barrier Alterations in MDX Mouse, An Animal Model of the Duchenne Muscular Dystrophy
Current Neurovascular Research EDITORIAL (Thematic Issue: New Targets of Medical Treatment in Psychiatric Disorders)
Current Neuropharmacology Protein Misfolding and Misprocessing in Complex Disease
Protein & Peptide Letters Structure and Function of the Acidic Ribosomal Stalk Proteins
Current Protein & Peptide Science Relative Hypermetabolism of Vermis Cerebelli in Traumatic Brain Injured Patients Studied with 18FDG PET: A Descriptor of Brain Damage and a Possible Predictor of Outcome
Current Radiopharmaceuticals Abnormal Striatal Dopamine Transmission in Schizophrenia
Current Medicinal Chemistry fMRI Simulator Training to Suppress Head Motion
Neuroscience and Biomedical Engineering (Discontinued) Mini-Review: Spinocerebellar Ataxias: An Update of SCA Genes
Recent Patents on DNA & Gene Sequences Preventive and Protective Roles of Dietary Nrf2 Activators Against Central Nervous System Diseases
CNS & Neurological Disorders - Drug Targets Going up in Smoke? A Review of nAChRs-based Treatment Strategies for Improving Cognition in Schizophrenia
Current Pharmaceutical Design Genetic Markers in Biological Fluids for Aging-Related Major Neurocognitive Disorder
Current Alzheimer Research Advances in the Research of β-Ketoacyl-ACP Synthase III (FabH) Inhibitors
Current Medicinal Chemistry Insights into the Role of Matrix Metalloproteinases and Tissue Inhibitor of Metalloproteinases in Health and Disease
Current Chemical Biology Mucopolysaccharidosis Type IVA (Morquio A Disease): Clinical Review and Current Treatment: A Special Review
Current Pharmaceutical Biotechnology Gene Therapy for Brain Cancer: Combination Therapies Provide Enhanced Efficacy and Safety
Current Gene Therapy Manufacturing Solid Dosage Forms from Bulk Liquids Using the Fluid-bed Drying Technology
Current Pharmaceutical Design Matter of Life and Death: the Pharmacological Approaches Targeting Apoptosis in Brain Diseases
Current Pharmaceutical Design Nutrition and Physical Activity on Hypertension: Implication of Current Evidence and Guidelines
Current Hypertension Reviews Editorial: Asleep at the Wheel: Concerning Driving after Co-Consumption of Alcohol and Benzodiazepines
Current Drug Abuse Reviews Clinical Trials for Neuroprotection in ALS
CNS & Neurological Disorders - Drug Targets